Different Inflammatory Signatures in Alzheimer’s Disease and Frontotemporal Dementia Cerebrospinal Fluid
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- Gustaf Boström
- Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden
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- Eva Freyhult
- Department of Medical Sciences, National Bioinformatics Infrastructure Sweden, Science for Life Laboratory, Uppsala University, Uppsala, Sweden
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- Johan Virhammar
- Department of Neuroscience, Neurology, Uppsala University Hospital, Uppsala, Sweden
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- Daniel Alcolea
- Memory Unit, Neurology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
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- Hayrettin Tumani
- Department of Neurology, Ulm University Hospital, Ulm, Germany
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- Markus Otto
- Department of Neurology, Ulm University Hospital, Ulm, Germany
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- Rose-Marie Brundin
- Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden
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- Lena Kilander
- Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden
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- Malin Löwenmark
- Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden
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- Vilmantas Giedraitis
- Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden
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- Alberto Lleó
- Memory Unit, Neurology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
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- Christine A.F. von Arnim
- Department of Neurology, Ulm University Hospital, Ulm, Germany
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- Kim Kultima
- Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden
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- Martin Ingelsson
- Department of Public Health and Caring Sciences, Geriatrics, Uppsala University, Uppsala, Sweden
Description
<jats:p>Background: Neuroinflammatory processes are common in neurodegenerative diseases such as Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but current knowledge is limited as to whether cerebrospinal fluid (CSF) levels of neuroinflammatory proteins are altered in these diseases. Objective: To identify and characterize neuroinflammatory signatures in CSF from patients with AD, mild cognitive impairment (MCI), and FTD. Methods: We used proximity extension assay and ANOVA to measure and compare levels of 92 inflammatory proteins in CSF from 42 patients with AD, 29 with MCI due to AD (MCI/AD), 22 with stable MCI, 42 with FTD, and 49 control subjects, correcting for age, gender, collection unit, and multiple testing. Results: Levels of matrix metalloproteinase-10 (MMP-10) were increased in AD, MCI/AD, and FTD compared with controls (AD: fold change [FC] = 1.32, 95% confidence interval [CI] 1.14–1.53, q = 0.018; MCI/AD: FC = 1.53, 95% CI 1.20–1.94, q = 0.045; and FTD: FC = 1.42, 95% CI 1.10–1.83, q = 0.020). MMP-10 and eleven additional proteins were increased in MCI/AD, compared with MCI (q < 0.05). In FTD, 36 proteins were decreased, while none was decreased in AD or MCI/AD, compared with controls (q < 0.05). Conclusion: In this cross-sectional multi-center study, we found distinct patterns of CSF inflammatory marker levels in FTD and in both early and established AD, suggesting differing neuroinflammatory processes in the two disorders.</jats:p>
Journal
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- Journal of Alzheimer's Disease
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Journal of Alzheimer's Disease 81 (2), 629-640, 2021-05-18
IOS Press
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Details 詳細情報について
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- CRID
- 1360576121956557824
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- ISSN
- 18758908
- 13872877
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- Data Source
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- Crossref